Details

Autor(en) / Beteiligte

• Neale, Benjamin M., Ph.D
• Medland, Sarah, Ph.D
• Ripke, Stephan, M.D
• Anney, Richard J.L., Ph.D
• Asherson, Philip, M.R.C.Psych., Ph.D
• Buitelaar, Jan, M.D
• Franke, Barbara, Ph.D
• Gill, Michael, M.B., Bch, BAO, M.D., MRCPsych, F.T.C.D
• Kent, Lindsey, M.D., Ph.D
• Holmans, Peter, Ph.D
• Middleton, Frank, Ph.D
• Thapar, Anita, M.D
• Lesch, Klaus-Peter, M.D
• Faraone, Stephen V., Ph.D
• Daly, Mark, Ph.D
• Nguyen, Thuy Trang, Dipl. Math. oec
• Schäfer, Helmut, Ph.D
• Steinhausen, Hans-Christoph, M.D., Ph.D., D.M.Sc
• Reif, Andreas, M.D
• Renner, Tobias J., M.D
• Romanos, Marcel, M.D
• Romanos, Jasmin, M.D
• Warnke, Andreas, M.D., Ph.D
• Walitza, Susanne, M.D
• Freitag, Christine, M.D., M.A
• Meyer, Jobst, Ph.D
• Palmason, Haukur, Ph.D
• Rothenberger, Aribert, M.D., Ph.D
• Hawi, Ziarih
• Sergeant, Joseph, Ph.D
• Roeyers, Herbert, M.D., Ph.D
• Mick, Eric, Sc.D
• Biederman, Joseph, M.D

Titel

Case-Control Genome-Wide Association Study of Attention-Deficit/Hyperactivity Disorder

Ist Teil von

• Journal of the American Academy of Child and Adolescent Psychiatry, 2010-09, Vol.49 (9), p.906-920

Ort / Verlag

Maryland Heights, MO: Elsevier Inc

Erscheinungsjahr

2010

Quelle

Applied Social Sciences Index & Abstracts (ASSIA)

Beschreibungen/Notizen

• Objective Although twin and family studies have shown attention-deficit/hyperactivity disorder (ADHD) to be highly heritable, genetic variants influencing the trait at a genome-wide significant level have yet to be identified. Thus additional genomewide association studies (GWAS) are needed. Method We used case-control analyses of 896 cases with DSM-IV ADHD genotyped using the Affymetrix 5.0 array and 2,455 repository controls screened for psychotic and bipolar symptoms genotyped using Affymetrix 6.0 arrays. A consensus SNP set was imputed using BEAGLE 3.0, resulting in an analysis dataset of 1,033,244 SNPs. Data were analyzed using a generalized linear model. Results No genome-wide significant associations were found. The most significant results implicated the following genes: PRKG1, FLNC, TCERG1L, PPM1H, NXPH1, PPM1H, CDH13, HK1 , and HKDC1. Conclusions The current analyses are a useful addition to the present literature and will make a valuable contribution to future meta-analyses. The candidate gene findings are consistent with a prior meta-analysis in suggesting that the effects of ADHD risk variants must, individually, be very small and/or include multiple rare alleles.